S.G. Priori (Silvia)http://repub.eur.nl/ppl/1604/
List of Publicationsenhttp://repub.eur.nl/eur_signature.pnghttp://repub.eur.nl/
RePub, Erasmus University RepositorySuicide attempts in a prospective cohort of patients with schizophrenia treated with sertindole or risperidonehttp://repub.eur.nl/pub/28228/
Wed, 01 Dec 2010 00:00:01 GMT<div>M.A. Crocq</div><div>D. Naber</div><div>M.H. Lader</div><div>F. Thibaut</div><div>M.D. Drici</div><div>B. Everitt</div><div>G.C. Hall</div><div>C. Le Jeunne</div><div>A. Mittoux</div><div>J. Peuskens</div><div>S.G. Priori</div><div>M.C.J.M. Sturkenboom</div><div>S.H.L. Thomas</div><div>P. Tanghøj</div><div>M. Toumi</div><div>R.D. Mann</div><div>N. Moore</div>
The incidence of suicide attempts (fatal and non-fatal) was analysed in a prospective cohort of patients with schizophrenia randomly assigned to sertindole (4905 patients) or risperidone (4904 patients) in a parallel-group open-label study with blinded classification of outcomes (the sertindole cohort prospective study - SCoP). The total exposure was 6978 and 7975 patient-years in the sertindole and risperidone groups, respectively. Suicide mortality in the study was low (0.21 and 0.28 per 100 patients per year with sertindole and risperidone, respectively). The majority (84%) of suicide attempts occurred within the first year of treatment. Cox's proportional hazards model analysis of the time to the first suicide attempt, reported by treating psychiatrists and blindly reviewed by an independent expert group according to the Columbia Classification Algorithm of Suicide Assessment (both defining suicide attempts by association of suicidal act and intent to die), showed a lower risk of suicide attempt for sertindole-treated patients than for risperidone-treated patients. The effect was statistically significant with both evaluation methods during the first year of randomized treatment (hazard ratios [95% CI]: 0.5 [0.31-0.82], p=0.006; and 0.57 [0.35-0.92], p=0.02, respectively). With classification by an independent safety committee using a broader definition including all incidences of intentional self-harm, also those without clear suicidal intent, the results were not significant. A history of previous suicide attempts was significantly associated with attempted suicides in both treatment groups. Safety of sertindole versus risperidone in schizophrenia: Principal results of the sertindole cohort prospective study (SCoP)http://repub.eur.nl/pub/21242/
Mon, 01 Nov 2010 00:00:01 GMT<div>S.H.L. Thomas</div><div>M.D. Drici</div><div>G.C. Hall</div><div>M.A. Crocq</div><div>B. Everitt</div><div>M.H. Lader</div><div>C.L. Jeunne</div><div>D. Naber</div><div>S.G. Priori</div><div>M.C.J.M. Sturkenboom</div><div>F. Thibaut</div><div>J. Peuskens</div><div>A. Mittoux</div><div>P. Tanghoj</div><div>M. Toumi</div><div>N.D. Moore</div><div>R.D. Mann</div>
Objective: To explore whether sertindole increases all-cause mortality or cardiac events requiring hospitalization, compared with risperidone. Method: Multinational randomized, open-label, parallel-group study, with blinded classification of outcomes, in 9858 patients with schizophrenia. Results: After 14147 person-years, there was no effect of treatment on overall mortality (sertindole 64, risperidone 61 deaths, Hazard Ratio (HR) = 1.12 (90% CI: 0.83, 1.50)) or cardiac events requiring hospitalization [sertindole 10, risperidone 6, HR = 1.73 (95% CI: 0.63, 4.78)]: Of these, four were considered arrhythmia-related (three sertindole, one risperidone). Cardiac mortality was higher with sertindole (Independent Safety Committee (ISC): 31 vs. 12, HR=2.84 (95% CI: 1.45, 5.55), P = 0.0022; Investigators 17 vs. 8, HR=2.13 (95% CI: 0.91, 4.98), P = 0.081). There was no significant difference in completed suicide, but fewer sertindole recipients attempted suicide (ISC: 68 vs. 78, HR=0.93 (95% CI: 0.66, 1.29), P = 0.65; Investigators: 43 vs. 65, HR=0.67 (95% CI: 0.45, 0.99), P = 0.044). Conclusion: Sertindole did not increase all-cause mortality, but cardiac mortality was higher and suicide attempts may be lower with sertindole.Who are the long-QT syndrome patients who receive an implantable cardioverter-defibrillator and what happens to them?: Data from the European Long-QT syndrome implantable cardioverter-defibrillator (LQTS ICD) registryhttp://repub.eur.nl/pub/27425/
Tue, 28 Sep 2010 00:00:01 GMT<div>P.J. Schwartz</div><div>C. Spazzolini</div><div>S.G. Priori</div><div>L. Crotti</div><div>A. Vicentini</div><div>M. Landolina</div><div>M. Gasparini</div><div>A.A.M. Wilde</div><div>R.E. Knops</div><div>I. Denjoy</div><div>L. Toivonen</div><div>G. Mönnig</div><div>M. Al-Fayyadh</div><div>L.J.L.M. Jordaens</div><div>M. Borggrefe</div><div>C. Holmgren</div><div>P. Brugada</div><div>L. de Roy</div><div>S.H. Hohnloser</div><div>P.A. Brink</div>
Background-: A rapidly growing number of long-QT syndrome (LQTS) patients are being treated with an implantable cardioverter-defibrillator (ICD). ICDs may pose problems, especially in the young. We sought to determine the characteristics of the LQTS patients receiving an ICD, the indications, and the aftermath. Methods And Results-: The study population included 233 patients. Beginning in 2002, data were collected prospectively. Female patients (77%) and LQT3 patients (22% of genotype positive) were overrepresented; mean QTc was 516±65 milliseconds; mean age at implantation was 30±17 years; and genotype was known in 59% of patients. Unexpectedly, 9% of patients were asymptomatic before implantation. Asymptomatic patients, almost absent among LQT1 and LQT2 patients, represented 45% of LQT3 patients. Patients with cardiac symptoms made up 91% of all study participants, but only 44% had cardiac arrest before ICD implantation. In addition, 41% of patients received an ICD without having first been on LQTS therapy. During follow-up, 4.6±3.2 years, at least 1 appropriate shock was received by 28% of patients, and adverse events occurred in 25%. Appropriate ICD therapies were predicted by age <20 years at implantation, a QTc >500 milliseconds, prior cardiac arrest, and cardiac events despite therapy; within 7 years, appropriate shocks occurred in no patients with none of these factors and in 70% of those with all factors. Conclusions-: Reflecting previous concepts, ICDs were implanted in some LQTS patients whose high risk now appears questionable. Refined criteria for implantation, reassessment of pros and cons, ICD reprogramming, and consideration for other existing therapeutic options are necessary. IK1 modulates the U-wave: insights in a 100-year-old enigmahttp://repub.eur.nl/pub/18403/
Sun, 01 Mar 2009 00:00:01 GMT<div>P.G. Postema</div><div>H.J. Ritsema van Eck</div><div>T. Opthof</div><div>G. van Herpen</div><div>P.F.H.M. van Pascal</div><div>S.G. Priori</div><div>C. Wolpert</div><div>M. Borggrefe</div><div>J.A. Kors</div><div>A.A.M. Wilde</div>
From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II.http://repub.eur.nl/pub/13247/
Tue, 14 Oct 2003 00:00:01 GMT<div>M. Naghavi</div><div>P. Libby</div><div>E. Falk</div><div>S.W. Casscells</div><div>S. Litovsky</div><div>J. Rumberger</div><div>J.J. Badimon</div><div>C. Stefanadis</div><div>P.R. Moreno</div><div>G. Pasterkamp</div><div>Z. Fayad</div><div>P.H. Stone</div><div>S. Waxman</div><div>P. Raggi</div><div>M. Madjid</div><div>A. Zarrabi</div><div>A.E. Burke</div><div>C. Yuan</div><div>P.J. Fitzgerald</div><div>D.S. Siscovick</div><div>C.L. de Korte</div><div>M. Aikawa</div><div>K.E. Juhani Airaksinen</div><div>G. Assmann</div><div>C.R. Becker</div><div>J.H. Chesebro</div><div>A. Farb</div><div>Z.S. Galis</div><div>C. Jackson</div><div>I.K. Jang</div><div>W. Koenig</div><div>R.A. Lodder</div><div>K. March</div><div>J. Demirovic</div><div>M. Navab</div><div>S.G. Priori</div><div>M.D. Rekhter</div><div>R. Bahr</div><div>S.M. Grundy</div><div>R. Mehran</div><div>A. Colombo</div><div>E. Boerwinkle</div><div>C. Ballantyne</div><div>W. Insull Jr</div><div>R.S. Schwartz</div><div>R. Vogel</div><div>P.W.J.C. Serruys</div><div>G.K. Hansson</div><div>D.P. Faxon</div><div>S. Kaul</div><div>H. Drexler</div><div>P. Greenland</div><div>J.E. Muller</div><div>R. Virmani</div><div>P.M. Ridker</div><div>D.P. Zipes</div><div>P.K. Shah</div><div>J.T. Willerson</div>
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.http://repub.eur.nl/pub/13244/
Tue, 07 Oct 2003 00:00:01 GMT<div>M. Naghavi</div><div>P. Libby</div><div>E. Falk</div><div>S.W. Casscells</div><div>S. Litovsky</div><div>J. Rumberger</div><div>J.J. Badimon</div><div>C. Stefanadis</div><div>P.R. Moreno</div><div>G. Pasterkamp</div><div>Z. Fayad</div><div>P.H. Stone</div><div>S. Waxman</div><div>P. Raggi</div><div>M. Madjid</div><div>A. Zarrabi</div><div>A.E. Burke</div><div>C. Yuan</div><div>P.J. Fitzgerald</div><div>D.S. Siscovick</div><div>C.L. de Korte</div><div>M. Aikawa</div><div>K.E. Juhani Airaksinen</div><div>G. Assmann</div><div>C.R. Becker</div><div>J.H. Chesebro</div><div>A. Farb</div><div>Z.S. Galis</div><div>C. Jackson</div><div>I.K. Jang</div><div>W. Koenig</div><div>R.A. Lodder</div><div>K. March</div><div>J. Demirovic</div><div>M. Navab</div><div>S.G. Priori</div><div>M.D. Rekhter</div><div>R. Bahr</div><div>S.M. Grundy</div><div>R. Mehran</div><div>A. Colombo</div><div>E. Boerwinkle</div><div>C. Ballantyne</div><div>W. Insull Jr</div><div>R.S. Schwartz</div><div>R. Vogel</div><div>P.W.J.C. Serruys</div><div>G.K. Hansson</div><div>D.P. Faxon</div><div>S. Kaul</div><div>H. Drexler</div><div>P. Greenland</div><div>J.E. Muller</div><div>R. Virmani</div><div>P.M. Ridker</div><div>D.P. Zipes</div><div>P.K. Shah</div><div>J.T. Willerson</div>
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.